Microstructural characteristics of chronic infarct segments assessed using diffusion tensor imaging

Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background The microstructural changes following myocardial infarction (MI) can be characterised in-vivo with cardiac diffusion tensor imaging (cDTI) imaging, using mean diffusivity (MD), fractional anisotropy (FA), secondary eigenvector angle (E2A) and helix angle (HA) maps. In this study, we use cDTI to explore the microstructural differences between subendocardial and transmural chronic infarct segments. Method Twenty STEMI patients (15 men, 5 women, mean age 59) underwent 3T CMR scan at 3 months following presentation (mean interval 107 ± 18 days). Scan protocol included: second order motion compensated (M012) free-breathing spin echo DTI (3 slices, 18 diffusion directions at b-values 100s/mm2[3], 200s/mm2[3] and 500s/mm2[12], acquired resolution was 2.20x2.27x8mm3; cine gradient echo and LGE imaging. Average MD, FA, E2A and HA parameters were calculated on a 16-AHA-segmental level. HA maps were described by dividing values into left-handed HA (LHM, -90° < HA < -30°), circumferential HA (CM, -30° < HA < 30°), and right-handed HA (RHM, 30° < HA < 90°) and reported as relative proportions. Infarct segments were identified using LGE; patients were categorised according to the maximal transmurality of their infarct segments, into subendocardial (<50% LGE) or transmural (>50% LGE) MI. Results DTI acquisition was successful in all patients (acquisition time 13 ± 5mins). Ten patients had transmural MI. The results are shown in table 1. Transmurally infarcted segments had significantly lower FA (FA subendocardial MI = 0.27 ± 0.04, FA transmural MI = 0.23 ± 0.02, p < 0.01), lower E2A (E2A subendocardial MI = 47 ± 7°, E2A transmural MI = 38 ± 6°, p < 0.01) and lower proportions of right-handed cardiomyocytes (RHM subendocardial MI = 21 ± 5%, RHM transmural MI = 14 ± 5%, p < 0.01) than subendocardial infarct segments. Conclusion Compared to subendocardial MI segments, the diffusion of water molecules is more isotropic in transmurally infarcted myocardium as evidenced by lower FA values, signifying increased structural disarray. The significantly lower E2A values suggest that laminar sheetlets of transmural infarct segments remain fixed at shallower angles during systole and are unable to reach their usual contractile configuration. The lower proportions of RHM on HA maps highlight the significantly greater loss of subendocardial cardiomyocytes in transmural infarct segments. Further studies are required to assess if these segmental changes can be predictive of long-term LV remodelling.

P1111Arrhythmogenic substrate detection in ischemic patients undergoing ventricular tachycardia ablation using multi-detector computed tomography: compared evaluation with cardiac magnetic resonance

Background Cardiac magnetic resonance (CMR) is capable of accurately identifying arrhythmogenic substrate (AS), leading to longer arrhythmia-free survival when used to guide ventricular tachycardia (VT) substrate ablation procedures. However, the use of CMR may be limited in certain centers or patient subsets. Purpose To evaluate the performance of multidetector cardiac computed tomography (MDCT) imaging in identifying heterogeneous tissue channels (HTCs) detected by CMR in ischemic patients undergoing VT substrate ablation. Methods Thirty ischemic patients undergoing both CMR and MDCT before VT substrate ablation were included. Using a dedicated post-processing software, two blinded operators, assigned either to CMR or MDCT analysis, characterized the presence of CMR- and CT-channels, respectively. CMR-channels were classified as endocardial (layers <50%), epicardial (layers ≥50%) or transmural. CMR- vs. CT-channel concordance was considered when the orientation was the same and they were located in the same AHA segment. Results Mean age was 69 ± 10 years; 90% were male. Mean left ventricular ejection fraction (LVEF) was 35 ± 10%. All patients had CMR-channels (n = 76), whereas only 26/30 (86.7%) had CT-channels (n = 91). Global sensitivity (Se) and positive predictive values (PPV) for detecting CMR-channels were 61.8% and 51.6%, respectively. MDCT performance improved in patients with epicardial CMR-channels (Se 80.5%), and transmural scars (Se 72.2%). In 4/11 (36%) patients with subendocardial MI, MDCT was unable to identify the AS. Conclusion MDCT fails to detect the presence of AS in 36% of patients with subendocardial MI and shows a modest sensitivity identifying the presence of HTCs, although its performance improves in patients with transmural scar. Abstract Figure. Multimodality imaging AS detection

INCREASED PLASMA CONCENTRATION OF CROSSLINKED FIBRIN POLYMERS IN ACUTE MYOCARDIAL INFARCTION

Thrombin cleaves fibrinopeptides from fibrinogen, converting it to fibrin monomer, and activates factor XIII which catalyzes the formation of intermolecular e-(y-glutamyl)-lysine bonds to stabilize the fibrin polymer. The formation of factor XIIIa-catalyzed fibrin polymers during clotting of plasma and purified fibrinogen in vitro was followed using an SDS agarose gel electrophoretic technique with radiolabeled antifibrinogen antibody overlay. Prior to clot formation an increase in both total amount and sizes of crosslinked fibrin polymers was demonstrated with at least 10 distinct polymeric forms identifiable by a time corresponding to .92 of the clotting time. Soluble polymers were shown to be crosslinked through y dimer formation by two dimensional electrophoresis with proportionately more dimer in each successively larger polymer. Plasma from patients initially presenting with acute myocardial infarction (MI) showed increases in the plasma concentration of fibrin polymer and in the proportion of total fibrinogen present as polymer, as determined by a quantitative adaptation of the electrophoretic technique. The plasma concentration of crosslinked fibrin dimer in patients with subendocardial or transmural MI showed significant (p <.005) increases to 4.0 ± 1.0% and 3.6 ± .8%, respectively, as compared to the concentration in normal plasma (.8 ± .1%). No difference in plasma concentration of fibrin polymer was found in samples from patients with transmural compared to subendocardial MI. This study provides the first direct demonstration and quantitation of factor XIIIa crosslinked fibrin polymers in thrombotic disease and the findings are indicative of increased activity of both thrombin and factor XIIIa in acute MI.